The proposed reseaach concerns the mechanisms of Na-Ca interactions in intenstinal and vascular smooth muscle. The smooth muscle preparations are the isolated guinea pig taenia coli, the rabbit aorta and the dog coronary artery. I will test the hypothesis of the plasmalemmal Na-Ca exchange carrier in a definitive way be measuring: (1) 45Ca efflux and net Ca extrusion as a function of external Na concentration ( (Na ion) 0), (2) Ca influx and net uptake as a function of (Na ions) in, (3) 22Na efflux and net extrusion as a function of (Ca2 ion)0 and (4) Na influx and net uptake as a function of (Ca2 ion) in. These experiments have become practical in my laboratory because of our long experience with measuring cellular Ca and my recent significant improvements of the quenching techniques for measuring both total intracellular Na ion and Ca2 ion. Using these techniques we are able to accurately measure the rate constant for net Ca extrusion against the electrochemical gradient from Ca loaded smooth muscle cells. This "active" Ca extrusion will be quantitated with respect to (a) the electrochemical Na ion gradient, (b) cellular ATP, (c) cellular cyclic AMP, (d) temperature, (e) electrochemical Ca2 ion gradient. In addition I will test the effect of intracellular Na on agonist sensitive cellular Ca compartments. The proposed research will provide a much needed quantitative description of the active Ca transport mechanism and its modulation by Na positive ions and a better understanding of Na-Ca interactions at other sites and their role in the control of smooth muscle contractility. This information will be of great importance in our understanding of the etiology of clinical hypertension.